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accession-icon SRP055573
RNA-seq of zebrafish brain, liver and skin during perturbation with rotenone at young and old age
  • organism-icon Danio rerio
  • sample-icon 68 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Zebrafish of two different age groups (12 and 36 months) were treated with low amounts of rotenone (mild stress) and compared to untreated zebrafish. Two different durations were used (3 and 8 weeks). Illumina sequencing (HiSeq2000) was applied to generate 50bp single-end reads. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de) Overall design: 68 sample: 3 tissues (brain, liver, skin); 2 age groups (12 and 36 months); controls and rotenone treated samples; 2-6 biological replicates for each group

Publication Title

Longitudinal RNA-Seq Analysis of Vertebrate Aging Identifies Mitochondrial Complex I as a Small-Molecule-Sensitive Modifier of Lifespan.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE46532
Stage-specific regulation of reprogramming to iPSCs by Wnt signaling and Tcf proteins
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon

Description

Wnt signaling is intrinsic to mouse embryonic stem cell self-renewal. Therefore it is surprising that reprogramming of somatic cells to induced pluripotent stem cells (iPSCs) is not strongly enhanced by Wnt signaling. Here, we demonstrate that active Wnt signaling inhibits the early stage of reprogramming to iPSCs, while it is required and even stimulating during the late stage. Mechanistically, this biphasic effect of Wnt signaling is accompanied by a change in the requirement of all four of its transcriptional effectors: Tcf1, Lef1, Tcf3, and Tcf4. For example, Tcf3 and Tcf4 are stimulatory early but inhibitory late in the reprogramming process. Accordingly, ectopic expression of Tcf3 early in reprogramming combined with its loss-of-function late enables efficient reprogramming in the absence of ectopic Sox2. Together, our data indicate that the step-wise process of reprogramming to iPSCs is critically dependent on the stage-specific control and action of all four Tcfs and Wnt signaling.

Publication Title

Stage-specific regulation of reprogramming to induced pluripotent stem cells by Wnt signaling and T cell factor proteins.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE31797
Activation of SREBP in Alveolar Type II Cells Enhances Lipogenesis Causing Pulmonary Lipotoxicity
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Background: Lung function is dependent upon the precise regulation of the synthesis, storage, and catabolism of tissue and alveolar lipids.

Publication Title

Activation of sterol-response element-binding proteins (SREBP) in alveolar type II cells enhances lipogenesis causing pulmonary lipotoxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE15293
Gene expression profiling of temporal lobes of wfs1 deficient mice
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon

Description

Aim of present study was to describe the changes induced deletion of the Wfs1 gene in the temporal lobe of mice. Mutant mice were backcrossed to two different genomic backgrounds in order to exclude confounding foreign genomic background influence. Samples from temporal lobes were analyzed by using Affymetrix Genechips, expression profiles were functionally annotated by using GSEA and Ingenuity Pathway Analysis. We found that Wfs1 mutant mice are significantly smaller (20.9 1.6 g) than their wild-type counterparts (31.0 0.6g, p < 0.0001). Interestingly, genechip analysis identified growth hormone transcripts up-regulated and functional analysis found appropriate pathways activated. Moreover, we found significant increase in the level of IGF1 in the plasma of wfs1 mutant mice. Taken together, wfs1 mutation induces growth retardation whereas the growth hormone pathway is activated. Further studies are needed to describe biochemical and molecular details of the growth hormone axis in the wfs1 mutant mice.

Publication Title

Wfs1 gene deletion causes growth retardation in mice and interferes with the growth hormone pathway.

Sample Metadata Fields

Specimen part

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accession-icon GSE25100
Expression data from CD19-positive splenic B cells isolated from 1-month old ID4+/-TCL1-tg and ID4+/+TCL1-tg mice
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The function of ID4 in CLL development was studied in vivo using TCL1 transgenic mouse model that develop leukemia similar to human CLL. TCL1 mice with ID4 single knockout gene have accelerated CLL progression.

Publication Title

Silencing of the inhibitor of DNA binding protein 4 (ID4) contributes to the pathogenesis of mouse and human CLL.

Sample Metadata Fields

Specimen part

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accession-icon GSE16104
IL-1b responses in receptor-reconstituted AcP-deficient neurons
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

The purpose was to determine AcP- and AcPb-dependent gene responses to IL-1 by virally-reconstituting AcP-deficient mouse embryonic cortical neurons with CD25 (control), full length AcP, AcPb or the combination of both. A control population was transduced with a CD25-expressing virus. Half the samples were stimulated with IL-1-beta for four hours, RNA was analyzed by microarray.

Publication Title

A central nervous system-restricted isoform of the interleukin-1 receptor accessory protein modulates neuronal responses to interleukin-1.

Sample Metadata Fields

Specimen part

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accession-icon GSE36826
Neutrophil-derived IL-1 is sufficient for abscess formation in immunity against Staphylococcus aureus in mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils.

Publication Title

Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.

Sample Metadata Fields

Specimen part

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
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Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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